Ventricular tachycardia (VT) is one of the most difficult management challenges in clinical cardiac electrophysiology. The spectrum of ventricular arrhythmias spans a wide range of clinical presentations that include premature ventricular complexes (PVCs), non-sustained ventricular tachycardia (NSVT), sustained ventricular tachycardia (VT) and ventricular fibrillation (VF). Any of these presentations can occur in patients with or without structural heart disease. This spectrum applies to any source of tachycardia originating below the His bundle whether from the bundle branches, Purkinje fibers or ventricular myocardium.
VT most commonly occurs in the setting of structural heart disease, such as coronary artery disease, heart failure, cardiomyopathy, congenital heart disease or following cardiac surgery. Prior myocardial infarction (MI) is by far the most common cause of sustained VT. Ventricular tachyarrhythmia associated with MI occurs in two stages. During the acute phase of MI, polymorphic ventricular tachycardia that can degenerate into ventricular fibrillation is most common. On the other hand, sustained monomorphic VT generally arises from the anatomic substrate of a healed MI that usually develops within 2 weeks after an MI and remains indefinitely. This substrate of healthy and damaged myocardium interlaced with fibrous tissue is found primarily at the border zone of the scar. Fibrosis creates areas of conduction block and increases the separation of myocyte bundles, slowing conduction through myocyte pathways in the border zone of the infarct thus creating a substrate that supports re-entry when an appropriate trigger occurs. With present management of MI, the incidence of sustained post-infarction VT is low, and fewer than 5% of acute MI survivors have inducible ventricular tachycardia when studied early after the acute event. VT exits the scar into the healthy myocardium and depolarizes the myocardium sequentially from this exit site. The location of the exit is responsible for the morphology of the ECG signal.
Sustained monomorphic VT occurring in the absence of structural or electrical heart disease is called idiopathic VT. Idiopathic VT can arise from different sites, but the right ventricular outflow tract (most commonly within 1-2 cm of the pulmonary valve) is by far the most common and accounts for approximately 10% of VTs seen by specialized arrhythmia services. Other potential sites include the left ventricular outflow tract, aortic sinuses of Valsalva (most commonly left) from a crescent of ventricular epicardium underlying the base of the sinus at the aortoventricular junction, in the endocardium adjacent to the mitral annulus and finally from the left ventricular epicardium remote from the sinuses of Valsalva, at sites adjacent to the coronary vasculature. These idiopathic VTs usually have a focal origin caused by triggered activity or abnormal automaticity.
Suppression of VT may be accomplished with the use of implantable cardioverter-defibrillators (ICDs), anti-arrhythmic drugs, arrhythmia surgery and catheter ablation. While antiarrhythmic drugs are considered first line therapy and are commonly used to complement therapy, they are not completely effective in preventing VT episodes and may cause significant cardiac and non-cardiac side-effects. ICD is the only treatment modality that has been demonstrated to offer a significant reduction in mortality in patients with scar-related VT. Although implantable cardioverter-defibrillators (ICDs) can improve the prognosis for patients with VT, recurrent VT can still be life-threatening. Catheter ablation offers a curative treatment for certain types of idiopathic VT and has been suggested to have a benefit for patients who have suffered prior MI in many case studies.
Cardiac mapping refers to all procedures involving recording of body-surface electrocardiograms or endocardial/epicardial electrograms generated due to the spread of the cardiac action potential. This can be recorded from the body surface using either conventional 12-lead electrocardiogram (ECG) or multiple leads (such as for body surface potential mapping (BSPM)), the endocardium or the epicardium. Cardiac mapping provides a means of visualizing the pathophysiological mechanisms underlying ventricular tachycardia, which is crucial for directing catheter ablation procedures.
Several conventional and advanced mapping techniques are frequently utilized to accomplish a successful catheter ablation. However, many of these mapping techniques are hampered by either hemodynamic instability or non-sustained nature of some tachycardias.
Conventional endocardial mapping techniques with catheters placed percutaneously into the heart chambers continue to be the most popular cardiac mapping modality. These catheters are localized and navigated using fluoroscopy. Several conventional mapping techniques have been developed over the last few decades to help understanding the mechanisms of arrhythmias and to guide catheter ablation. These conventional mapping techniques include activation mapping, pacemapping and entrainment mapping.
Pacemapping is a commonly used tool for mapping non-sustained or hemodynamically unstable VT; it is based upon the principle that activation of the heart from a given site will yield a reproducible body surface electrocardiogram (ECG) morphology and that pacing from a site very close to the site at which VT activates the heart (i.e. the site of origin) will result in a matching ECG morphology. However, this technique has some limitations. Comparison of the 12-lead ECG morphology between a pace-map and clinical tachycardia is frequently completely subjective or semi-quantitative. Discrepancies in ablation results may result, in part, from subjective differences in the opinion of a pace-map match to the clinical tachycardia. Another important limitation is that increasing the strength to pace diseased tissues, as in scar-related VT, can excite tissues more distant to the area of stimulation (even if unipolar pacing is used) which may lead to a 12/12 match even 1-1.5 cm away from successful ablation sites. This technique is therefore very time consuming and is limited by imperfect accuracy and spatial resolution, subjectivity of interpretation, and by the need for an intuitive interpretation of the ECG to direct catheter manipulation.
BSPM incorporates data from a much larger number of electrodes, but remains limited by the remote location of the recording site from the cardiac surface resulting in poor spatial resolution of electrical events. The recent development of electrocardiographic imaging (ECGI) represents a further refinement of this technique, combining BSPM and heart torso geometric information to produce detailed electroanatomical maps of the epicardial surface through application of inverse solution mathematical algorithms. This methodology has permitted accurate localization of focal activation sources, as well as detailed activation sequences during re-entrant arrhythmias. ECGI was recently used to assist in the diagnosis and guiding catheter ablation of focal idiopathic as well as scar related VT. A number of limitations are still under investigation, the most important being the accuracy, but also the complexity of the procedure and the need for a long processing time from electrocardiographic signal acquisition to 3D display of the derived epicardial potentials.
There is therefore a need for a system that assists in the localization of the site of origin.